Estrogen induces hyperlipidemia in fasted chicks.
To determine whether the estrogen-induced hyperlipidemia is affected by fasting, male growing chicks were administered subcutaneously a single dose of 17 beta-estradiol (25 mg/kg body wt), and the hormone treatment lasted for 2 days with or without feed (Experiment 1). In the second experiment, chicks were initially fasted for 1 or 3 days, and then treated with the same dosage of 17 beta-estradiol as in Experiment 1 for 2 days without feed. Plasma and liver lipids, and the activities of hepatic malic enzyme, glucose-6-phosphate dehydrogenase, and hormone-sensitive lipase in the adipose tissue were determined. Compared with fed control chicks, estrogen treatment in fed birds resulted in a marked elevation of plasma lipids, especially triglyceride during the 2-day period (137 vs 2263 mg/dl). In fasted chicks, the present finding that estrogen also induced a marked hyperlipidemia is noteworthy. Upon estrogen treatment (Experiment 1), the level of plasma triglyceride in fasted birds increased about 16 times over that of the fasted control group (133 vs 2093 mg/dl). Even in chicks fasted for 5 days (Experiment 2), estrogen treatment resulted in a persistent hypertriglyceridemia (75 vs 1369 mg/dl). In fed chicks, estrogen treatment also induced a fatty liver with massive accumulation of triglyceride, but the liver of estrogen-treated/fasted chicks appeared to be normal. In both fed and fasted chicks, malic enzyme was found to be the major NADPH producing enzyme in the liver. Upon fasting, both malic enzyme and glucose-6-phosphate dehydrogenase activities decreased significantly (P less than 0.05). In fed chicks, the total activities of both enzymes increased with estrogen treatment, whereas the effect of hormone on these enzymes was less obvious in fasted chicks. The hormone-sensitive lipase activity in the adipose tissue was much lower in fed chicks compared with that of fasted birds (0.15 vs 0.33 nmol of oleic acid released/min/mg protein). Estrogen treatment in fed chicks had no effect on the hormone-sensitive lipase activity, but its activity was enhanced by the hormone treatment in fasted chicks. The present finding that hyperlipidemia persisted in estrogenized chicks during the fasting seems to indicate the complex nature of this hormonal influence on lipid metabolism.
Cho
B H
BH
Harlan E. Moore Heart Research Foundation, Champaign, Illinois 61820.
Park
J R
JR
D000273:Adipose Tissue / Q000201:enzymology; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D002645:Chickens; D002784:Cholesterol / Q000097:blood; D004967:Estrogens / Q000494:pharmacology*; D005215:Fasting; D005954:Glucosephosphate Dehydrogenase / Q000032:analysis; D006949:Hyperlipidemias / Q000209:etiology*; D008049:Lipase / Q000032:analysis; D008055:Lipids / Q000032:analysis; D008099:Liver / Q000032:analysis / Q000201:enzymology / Q000254:growth & development; D008291:Malate Dehydrogenase / Q000032:analysis; D008297:Male; D009929:Organ Size; D010743:Phospholipids / Q000097:blood; D011897:Random Allocation; D014280:Triglycerides / Q000097:blood
D001786:Blood Glucose; D004967:Estrogens; D008055:Lipids; D010743:Phospholipids; D014280:Triglycerides; D002784:Cholesterol; D008291:Malate Dehydrogenase; D005954:Glucosephosphate Dehydrogenase; D008049:Lipase